The Biology Blogger

What happens when you have a really great medication to try and treat spinal chord and brain injuries, but you can’t get it to the part of the body? You are left with a medication that can’t be used and injuries that go untreated. But, what happens when you pull in a growing field of chemistry (that happens to be my chemistry professor’s interest) and throw it into the medical field?

You wind up with a mix of medicine and nanotechnology that results in the possibility to treat brain and spinal chord injuries. Researchers, led by Richard Borgen at Purdue University, developed a method of treatment which allows for the transport of medications to the brain and spinal chord by using silica nanoparticles.

Previous to studying the use of nanoparticles on medication transfer, Borgen and his team studied the effects of polyethylene glycol (PEG). What the team found was that PEG helped to treat rats with brain damage and dogs with spinal chord injuries. The way that PEG works is that it targets the damaged cells and seals the area that is injured. According to Borgen, it also restores cell function.

But, what Borgen and his team found was that if you dilute it too much, you can turn it into ethylene glycol which is found in antifreeze. That’s toxic. And, if they didn’t dilute it enough, it turned into a very viscous liquid which is hard for injections. So, despite the fact that the team found the great benefits of PEG, they were unable to use it to the max degree.

But, they found that if they coated silica nanoparticles with PEG, they could transport it right to the part of the body that needed repairing. Because nanoparticles are so tiny (some as small as a large virus), the ability to inject as many as they need became a real possibility. There are tiny holes in the nanoparticles that, when they have reached their destination, release the medicine.

I don’t know much about nanotechnology other than the fact that the things they are dealing with are incredibly tiny. But, I have always held the opinion that the trick to curing problems is not the big route, but the tiny route. By coating these nanoparticles, they are making it so that they can send as much medicine to the problem as they need to.

Do I think this is good research? Yes. But, the big argument I can see being presented is: how much would all these nanoparticles cost? Is there a considerable cost to producing nanoparticles? Weighing the pluses and minuses will definitely happen.

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For some time now, scientists knew that tiny snippets of RNA called “microRNA” were found in the body and aided the DNA in creating much needed proteins.  But, as scientists researched this microRNA, they found that it was located only in certain places: the cardiovascular system.  What this suggested to scientists was that microRNA was directly connected to the cardiovascular system and more importantly, its development.

To study this, scientists took miR-126.  The reason they chose this is because miR-126 is only found in endothelial cells.  Endothelial cells line the inside of blood vessels and are responsible for so many different things: the development of new blood vessels in embryos, the repair of injured blood vessels, and the creation of blood vessels to support growing tumors.  That last part is what is most interesting.

Scientists found when studying mice that when they removed miR-126 from the mice, 40% died almost immediately after birth or even before birth.  They found that the remaining that did make it to adulthood were able to live fine as if nothing had happened.  But, when scientists simulated a heartattack, those that lacked the miR-126 were unable to survive which suggests that miR-126 is only necessary for development and then when there is severe damage done to the blood vessels.

Another study that they conducted was on aortial cut sections.  They wanted to study the branching of blood vessels that occured when there was and was not miR-126 in the tissue.  Scientists found that when there was, branching occured regularly.  But, when there was no miR-126, branching did not take place nearly as much as when there was miR-126.

What this suggests is a lot of potential therapies for those that have heart problems.  By being able to manipulate miR-126 and numerous other microRNAs, scientists might be able to stop certain cancers from coming as well.  As I stated earlier in the article, endothelial cells are responsible for creating new blood vessels to tumors.  Well, if you get rid of miR-126, endothelial cells which line the inside of those blood vessels won’t exist and the vessel, therefore, won’t be able to supply blood to the tumor.  No blood, no tumor.

What do you think, though?  Do you think that this is a new, great way of potentially treating cancer or do you think it’ll last for a week and then something new and greater will come along?  Leave a comment letting us know!

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Epilepsy is a neurological disorder that can be characterized by repeat, unprovoked seizures.  It is a common disorder with over 50,000 people having it at one point or another.  Unfortunately, it can not be cured and therefore, must be treated with a constant use of different medications.  One of those medications is topiramate.  Topiramate is an epilepsy drug that doubles as a migraine medication.  What scientists found, though, disturbed them.

A study was conducted on women who got pregnant while on topiramate both on its own or along with another drug.  What they found was incredibly upsetting.  Out of 178 babies born, 16 of them had severe birth defects.  Three of these babies came from mothers who only took topiramate.  The other thirteen came from mothers who took topiramate and other epilepsy drugs.  Four babies had cleft lips in this study which was eleven times more than what normally would happen.  And four of the boys had genital birth defects.

Researchers, though, understand that they need to do more research to really determine just how horrible the effects of topiramate are on babies.  Furthermore, since topiramate is used for both epilepsy and migraines, the question that pops into their heads is whether there is a difference in birth defects if it is used for migraine purposes rather than for epilepsy purposes.  Regardless, if it is causing these birth defects, researchers need to get more information so it can be taken off the market.

If a drug causes harm such as this, it needs to be removed from the market.  We need to stop letting these pharmaceutical companies put out these harmful drugs just because their bottom lines are important.  If this drug does do harm, it needs to be removed from the market.  But, what do you think?  Looking at the results, do you think that it was some freak accident or do you think that topiramate really is causing this?  Regardless of what you feel, I do think that more research should be done on a larger scale.  Rather than under 200 woman, try one thousand or even more.  If there is a bigger study group, the results will be better.

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When we get a cold, we are sick for a few days and then, over time, we get better.  The virus runs its course and the body finally beats it.  Even if we get the flu, the same thing happens.  For so long, there was this back and forth struggle between humans and viruses to see who was the dominant.  The virus would evolve thus forcing the human to evolve thus forcing the virus to evolve and it was a continuous struggle back and forth for thousands of years.  Now, though, scientists seem to have found a protein that originated millenia ago.

Called APOBEC3G, this protein is effective in changing the DNA around on a virus thus making it inactive.  But, before they knew about the APOBEC3G, the researchers used a virus called HERV-K to see just what it could do to modern day cells.  See, it’s a retrovirus that had not been around for a long time.  What the scientists found was that numerous different immune response molecules were released to try and destroy the virus.  What they found, though, was the release of APOBEC3G had its lasting effect, even today, on the old virus.

What does this mean, though?  It means that we have held on to some of the things that evolved with us even after so many thousands of years.  It can be assumed then that because of our war with viruses thousands of years ago, we are now stronger and more capable of going against them these days.  Although that is not always the case, it is interesting to see these molecules pop up that were not always there and then appeared and now are there permanately.

This is exciting because it is a first hand experience of, as the researcher put it, the battle between host and virus.  Who will win, though?  The battle continues to wage…One day the virus is stronger and then suddenly, the human evolves a bit and changes and adapts, thus making him/her immune to the virus.  And back and forth.  It is interesting to see the very definite appearance of a molecule that was used so long ago still being used today.  I wonder what else they may find when testing viruses vs. human cells.

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Scientists from Canada and Europe have recently come across some findings that are incredibly interesting and, more importantly, very important to women.  What scientists found was one of the genes responsible for the regulation of ovulation.  In essence, this gene is required for the woman to ovulate.  Without it, the woman won’t ovulate and the rest is history.  Called the Lrh1 gene, this gene has become a very interesting source of information for the scientists.

What they did was took a mouse and genetically modified it so that the Lrh1 gene was turned off.  What they found was that this mouse, when her gene was turned off, did not ovulate.  In essence, no matter what reproduction happened, there would be no egg there to fertilize.  The reason this finding is so interesting is because of the pharmaceutical reasons.  There is a lot of money to be made in the ability to turn off the Lrh1 gene.

But more importantly and my reason for finding it so interesting is its contraceptive methods.  Current contraceptive plays around with the hormones, making the body believe its pregnant.  However, it’s not full proof.  If you are able to turn off the gene that causes ovulation, you won’t release an egg.  Without an egg, there’s no fertilization.  Without fertilization, there’s no baby.

Fortunately, there’s more than just the contraceptive behind it.  While scientists can synthesize a drug that can be used to prevent pregnancy, they can go the other way as well and create a therapy that will make the gene work again.  By doing that, women that were, at one time, infertile because they could not ovulate can suddenly ovulate all over again.  This will make women couldn’t have babies suddenly get that miracle of life.

I love science, but sometimes, something comes along that is just really nice to know.  There are few side effects, scientists hope, from turning off the hormone so the contraceptive side of things is great.  And, add the fact that they might be able to create a therapy to increase the chances of a woman getting pregnant and you really find that these findings are really quite interesting.  What do you think, though?  Is it a good idea or a bad idea to play around with this gene?

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When we hear a story about a gene variation that makes a person immune to malaria, people get excited. But, how excited would people be if that same gene that makes people immune to one disease left them more susceptible to another disease? I don’t know how excited we’d be. Unfortunately, that’s happened. According to an article I read at the New York Times, those in Africa that developed a gene that allowed for an immunity against an ancestor to the modern day malaria are more prone to get HIV.  Alone, this gene could be the cause of 11% of the cases of HIV.

The question people are asking is: why is it when one disease is protected against, the other becomes more likely to infect the person?  The answer to that lays on the receptors of the red blood cells and the white blood cells.  Malaria attaches to a receptor that is found on red blood cells.  This receptor is meant to attach to a hormone called CCL5.  About 10,000 years ago, humans in Africa stopped having those receptors and they suddenly stopped getting malaria.

Now that HIV is around, though, one scientist suddenly had a realization.  Robin Weiss is a biologist at University College of London.  He found that HIV was using red blood cells to get around the body in particular patients.  Instead of the malaria attaching to the receptor, the HIV attaches to the receptor.  And what you get is a case of increased HIV infections.  It sounds confusing?  It is.  Scientists realized that if there is a lack of this one receptor on the red blood cells, HIV increases.  If there is a lack of the receptor on the white blood cells, HIV goes away.  It’s confusing.

What does this all mean, though?  It explains why HIV is so dangerous in Africa.  More importantly, though, it gives more information into understanding about the biology behind HIV.  We don’t know much about HIV.  It’s relatively new so we can’t do genetic research.  That’s irritating for scientists because if we knew about the genome, we might be able to target it better.  This research, although very upsetting, could lead to more information on potentially finding a vaccine.  On an aside, a trial for a vaccine against HIV was just cancelled.

Hopefully we can find a cure for this virus.  But, right now, we just have more knowledge.  We are starting to understand more and more on how this virus works.  It’s not a lot, but it’s something.  Now all we need is to get a vaccine out, huh?

What do you get when you use antibiotics far too much for any old sickness?  Antibiotic resistant bacteria is what you get.  Why?  It’s very simple.  The bacteria learn how to defend against whatever that antibacteria is.  It’s the same for anything.  If you cough on me, I’m going to get sick.  When I get better, if someone with that exact same strand of sickness coughs on me, I won’t get sick.  I’ve grown immune to it.  The same happens for bacteria.  They get immune to what we use against them and then continue to wreck havoc.

For instance, methicillin-resistant Staphylococcus aureus (MRSA) is a super bug.  No longer can it be treated with beta-lactam antibiotics.  Sure, there are antibiotics to counter MRSA, but as bacteria get used to different treatments, they become more and more resistant.  Add the fact that bacteria reproduce like crazy and you get a very simple understanding on why we need to be worried about these resistances.  Fortunately, there is hope.

Rockefeller University scientists have found a way to target the gene in the bacteria that creates this resistance.  In essence, they made a drug that removed the gene’s ability to make the bacteria resistant.  By doing that, the bacteria can be destroyed.  Called Ceftobiprole, this drug was tesed against MRSA which kills more people in and out of hospitals than any of the other drug-resistant bacteria.  The results from this were phenomenal.  100% knock out of the bacteria.  Not 50%.  Not 99.9%.  All bacteria were knocked out.

But, this wouldn’t be an effective treatment if they didn’t try other bacteria as well.  So, the scientists tesed Ceftobiprole on VRSA which is another S. aureus strain that is resistant to vancomycin.  What they found was incredible.  Ceftobiprole knocked them out as well.  By knocking out the gene that allows the bacteria to adapt and become resistant, the antibiotic was able to do its job in destroying the bacteria.

This research is interesting…For so long, the way the game worked was we created an antibiotic, used it for a while, and then stopped using it because the bacteria had grown resistant.  In this case, the bacteria can’t grow resistant.  Therefore, we can see the scientists had played a different game than normal.  Instead of trying to find a way to destroy the bacteria, they found a way to stop its resistance.  Get rid of its defenses and it becomes even easier to destroy.

I think this can prove incredibly useful in a lot of bacterial infections.  I can’t think of any way that the bacteria can best this.  However, science shows that anything is possible and I know that these scientists will have to continue working to ensure that they stay one up on the bacteria.  In this game, scientists won.  Scientists 1 - Bacteria 0.

Source: Science Daily.

When certain signals in a cell start to alter and change, the cells undergo unusual levels of growth which result in tumors.  That’s all cancer really is…an unusual level of cell growth which results in a growth that can kill a person.  There are treatments for cancer, such as radiation and chemotherapy which targets and tries to destroy the cells that are growing in an unusual level.  However, that doesn’t always do it and it doesn’t get to the root of the problem: getting control of that signal that alters the growth of the cells.

Using rats, scientists have started to experiment and find a way in which they can find the ideal level of Myc (a signaling molecule that had a direct connection in the growth of cells).  Basically, if Myc is too low, the cells start to die out and if Myc is too high, the cells start to grow larger with no control and they become tumors.  In the past, scientists had experimented with just turning the Myc molecule off; however, they found that cells actually needed this to survive, so it was proven that turning it off just wouldn’t be a good idea.

What they did realize, though, was that when they tweaked the Myc molecule and just lowered the levels below the threshold that caused tumor growth, the cells actually returned to normal size.  For any scientist, this was probably a very exciting thing.  The importance of finding this threshold was pivotal because Myc exists in both healthy and unhealthy cells.  By figuring out what level was suitable for normal cells and what levels would trigger tumor growth, scientists are now able to figure out a medication that could be used for cancer treatment.

The way I see it, this is a really great way to try and cure cancer.  High levels of Myc is the cause of 50% of cancers.  If a drug were introduced that somehow lowered these levels below the threshold, the cells would naturally return to normal and start dying normally.  However, the thing that scientists need to be careful of is lowering it too much.  If the Myc is turned off completely, the cells will die.  It’ll be a bit of trial and error I am sure to try and find a way to lower the Myc effectively without lowering it too much.

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In the 80s, when HIV first started to appear, no one knew what to do about it.  As time went on, drugs started appearing that would help the patient with it, but would never get rid of it.  As more time went on, other drugs started appearing.  However, the fundamental cause of it and the ability for it to spread was never touched on.  There was nothing scientists could do.  If an infected person transmitted the virus to another person, chances are that person is going to get it.  However, scientists seem to have made a breakthrough that could lead to a new type of therapy for treating HIV patients.  Could it work?  Let’s first take a look at what they do.

As everyone knows, HIV targets the T-cells in our immune system.  It destroys them which is why if someone has it, they are more susceptible to other illnesses.  A person with HIV could die from a disease that would normally not cause any harm.  The thing about HIV is that it requires two receptors on the surface of the T-cell to get into that cell.  One of those is CCR5 which allows things to bind to it.  HIV uses this receptor to bind to the cell and then inject its genetic code to take over the cell.  Without this CCR5 receptor, though, HIV could not spread.  Science has found a way to disable that receptor.

By using a zinc finger protein, scientists are trying to promote mutations in the genetic code of this CCR5 receptor.  But, what is a zinc finger protein?  It is a type of protein that, specifically in this experiment, carries an enzyme to the receptor and breaks the genetic code.  When the repair process occurs for the genetic code, it repairs different than normal.  By doing this, the receptor effectively becomes disabled.  Without it, the HIV can’t transfer.  In essence, this is doing the same thing that a very rare number of people naturally have.  Basically, there are some people that are immune to HIV because their receptor is mutated.  Scientists are hoping that they can take these T-cells from the body and then alter them before putting them back in.  This ultimately creates an immunity to HIV.

Now comes the big question: can it really work?  When testing it out on mice that had AIDS, they used actual human cells.  What they found was after they had disabled the CCR5 receptor and followed the cells for some time, the viral load in that mouse reduced tremendously.  This group of researchers is now hoping to do a human trial in which they will take the T-cells from an HIV patient and then alter the CCR5 receptor before putting it back into them.  Their hopes?  To reduce that patient’s viral load.

I have doubts about this…First and foremost, what will happen if the HIV is removed from the patient?  The CCR5 receptor will still be disabled.  Will that patient then never have use of that receptor again?  Furthermore, on a more ethical stand point, who gets the treatment?  If you find a cure for HIV, you can charge as much as you want.  With Africa having such a high rate of HIV and AIDS, will they get any treatment?  I hope that this therapy does work, I really do.  I just wonder if there will be side effects.  I suppose the human trials will prove what side effects are.  Regardless, this is really a break through in HIV therapy and could prove life saving for so many millions.  Great work.

Earlier, I wrote about how the rise in temperature has caused a change in the type of fish in the Rhode Island Sound.  And I said in the article that the rise in the temperature on the Earth could impact us.  Well, it does.  West Nile Virus first appeared in 1999 as we all remember.  It was spread by mosquitoes and we were told to ensure that we didn’t keep damp environments around because of the fear of mosquitoes multiplying and then spreading West Nile.  That was a common fear, but it only spread even more when, in 2002, a new strand of West Nile Virus appeared.  By 2005, it had replaced the old strand and had caused numerous deaths.  Now, over 100 people a year die from this strand.

So, what happened?  How did this strand of West Nile Virus do so much damage while the other one didn’t?  And more importantly: how did it spread so fast?  Two scientists, Kilpatrick and Kramer, conducted an experiment to try and determine what effects temperature had on the spread of the virus and to try and determine when the virus can be transmitted by mosquitoes.  What the studies showed was that this new strand was much easier passed from mosquitoe to human than the old strand.  What they also found was that this new strand had a better advantage when the temperature increased.

Both strands were able to increase its spread when the temperature was higher.  What this means is that as the heat on the planet increases, the increased replicating of the virus will continue to rise and the spread of the virus will continue quickly.  This new strand is better at replicating in the mosquitoe because of the increased temperature, scientists suggest.  Now what they are looking to prove is whether or not the temperature had a connection in the new strain’s ability to invade so effectively.

A lot of people know about West Nile Virus…The increase in its ability to spread should be a warning call to people about the threat of global warming.  We’re told that global warming might melt the ice caps and that the water might rise.  Okay, that’s sort of a bothersome image.  But, because of global warming, we can suddenly see an increase in a disease.  This has a direct connection to us.  It’s not about fish this time…It’s about a disease that can kill humans.  And, if the virus continues to spread and replicate as fast as it is, it could start to kill more people.  Global warming is an issue…One that we, as a people, need to figure out a solution for.